Using the Drosophila visual neurons as a model, we study dendritic development in the central nervous system. Like vertebrate cortex and retina, the medulla neuropil in the Drosophila optic lobe is organized in columns and layers, suggesting that the fly medulla neurons and vertebrate cortex neurons confront similar challenges in routing their dendrites to specific layers and columns during development. In addition, the fly visual system has several unique advantages: (i) the medulla neurons extend dendritic arbors in a lattice-like structure, facilitating morphometric analysis; (ii) the presynaptic targets for many medulla neuron types have been identified from our anatomical studies and others; (iii) genetic tools for labeling specific classes of medulla neurons and determining their connectivity have been developed in our previous studies. We have developed several novel techniques to analyze dendritic structures in three-dimension (3D) space and to exploit the unique advantages of this system. (i) To image reliably the slender dendrites of medulla neurons, we developed a dual imaging technique that generates isotropic 3D-images of dendrites by combining two confocal image stacks collected in orthogonal directions. (ii) We developed an image registration technique that makes uses of the regular array structures of the optic lobe to standardize dendritic branching patterns. This, in combination with a series of statistical methods we established, allows us to analyze dendritic patterns in three-dimension space. (iii) We have developed a modified GRASP (GFP-reconstitution across synaptic partners) technique to detect bona fide synaptic connections at the light-microscopic level. Using these techniques, we first analyzed the dendritic morphologies of three types of medulla neurons, Tm2, Tm9 and Tm20. Tm20 receive input from R8 photoreceptors in their cognate columns and mediate color vision while Tm2 receives inputs from the achromatic R1-6 via L2 and L4 in its cognate columns and mediates motion detection. Our morphometric analyses revealed (i) that the medulla neurons exhibit stereotypic dendritic arbors but the detailed branching pattern and topology are not conserved; (ii) that the synaptic partnership between axons and dendrites are robust and specific; (iii) that the layer-specific routing and polarized extension of dendrites are two most critical determinants of type-specific dendritic patterns; (iv) that the dendritic arbors of these Tm neurons are largely confined to single medulla columns, consistent with their functions in processing retinotopic information; (v) the majority of the dendritic arbors are originated from one or two branching points that are located in specific medulla layers. In contrast, the Dm8 amacrine neurons form a wide dendritic field to cover multiple medulla columns and to receive 16 R7 photoreceptor inputs. Based on these results, we hypothesize that dendritic development in the optic lobe neurons proceeds in three distinct processes: (i) initiating dendritic extension from axons in specific layers; (ii) routing dendrites in type-specific fashion toward specific layers and in specific planar direction to elaborate an dendritic field of an appropriate size; (iii) matching different sections of dendrites with specific afferents, which likely requires specific interactions between axons and dendrites to ensure synaptic specificity. To determine the molecular mechanisms guiding dendritic development, we screened available mutants for their functions in Tm20 and Dm8 dendritic development. We found that mutations in the components of the TGF-beta/Activin signaling pathway affect the size of their dendritic fields. R7- and R8-photoreceptor-derived Activin selectively restricts the dendritic fields of their respectively postsynaptic partners, Dm8 and Tm20, to the size appropriate for their functions. We found that canonical Activin signaling promotes dendritic termination without affecting dendritic routing direction or layer. We showed that mutant Tm20 neurons lacking components of Activin signaling pathway expanded their dendritic fields and formed incorrect synapses with neighboring photoreceptors, thereby losing the one-to-one correspondence with R8s. Similarly, mutant Dm8 neurons devoid of Activin signaling over-expanded their dendritic field while mutant Dm8 neurons with overactive Activin signaling had dendritic fields of reduced sizes. Our finding that photoreceptor-derived Activin controls the dendritic development of their synaptic targets, suggests that anterograde signaling is an effective mechanism for coordinating afferent-target development late in development. The use of afferent-derived Activin to regulate dendritic patterning provides an adaptable and self-compensating mechanism for afferents to control the receptive field sizes of their synaptic partners.